Nanog signaling in cancer promotes stem-like phenotype and immune evasion
DC Field | Value | Language |
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dc.contributor.author | Noh, Kyung Hee | - |
dc.contributor.author | Kim, Bo Wook | - |
dc.contributor.author | Song, Kwon-Ho | - |
dc.contributor.author | Cho, Hanbyoul | - |
dc.contributor.author | Lee, Young-Ho | - |
dc.contributor.author | Kim, Jin Hee | - |
dc.contributor.author | Chung, Joon-Yong | - |
dc.contributor.author | Kim, Jae-Hoon | - |
dc.contributor.author | Hewitt, Stephen M. | - |
dc.contributor.author | Seong, Seung-Yong | - |
dc.contributor.author | Mao, Chih-Ping | - |
dc.contributor.author | Wu, T. -C. | - |
dc.contributor.author | Kim, Tae Woo | - |
dc.date.accessioned | 2021-09-06T13:51:28Z | - |
dc.date.available | 2021-09-06T13:51:28Z | - |
dc.date.created | 2021-06-15 | - |
dc.date.issued | 2012-11 | - |
dc.identifier.issn | 0021-9738 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/107078 | - |
dc.description.abstract | Adaptation of tumor cells to the host is a major cause of cancer progression, failure of therapy, and ultimately death. Immune selection drives this adaptation in human cancer by enriching tumor cells with a cancer stem cell-like (CSC-like) phenotype that makes them resistant to CTL-mediated apoptosis; however, the mechanisms that mediate CSC maintenance and proliferation are largely unknown. Here, we report that CTL-mediated immune selection drives the evolution of tumor cells toward a CSC-like phenotype and that the CSC-like phenotype arises through the Akt signaling pathway via transcriptional induction of Tcl1a by Nanog. Furthermore, we found that hyperactivation of the Nanog/Tcl1a/Akt signaling axis was conserved across multiple types of human cancer. Inhibition of Nanog in a murine model of colon cancer rendered tumor cells susceptible to immune-mediated clearance and led to successful, long-term control of the disease. Our fmdings establish a firm link among immune selection, disease progression, and the development of a stem-like tumor phenotype in human cancer and implicate the Nanog/Tcl1a/Akt pathway as a central molecular target in this process. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | AMER SOC CLINICAL INVESTIGATION INC | - |
dc.subject | TUMOR-INFILTRATING LYMPHOCYTES | - |
dc.subject | ANTITUMOR IMMUNITY | - |
dc.subject | VACCINE POTENCY | - |
dc.subject | SELF-RENEWAL | - |
dc.subject | HIGH NUMBER | - |
dc.subject | CELLS | - |
dc.subject | AKT | - |
dc.subject | ENHANCEMENT | - |
dc.subject | ACTIVATION | - |
dc.subject | RESISTANCE | - |
dc.title | Nanog signaling in cancer promotes stem-like phenotype and immune evasion | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Noh, Kyung Hee | - |
dc.contributor.affiliatedAuthor | Song, Kwon-Ho | - |
dc.contributor.affiliatedAuthor | Kim, Tae Woo | - |
dc.identifier.doi | 10.1172/JCI64057 | - |
dc.identifier.scopusid | 2-s2.0-84868618042 | - |
dc.identifier.wosid | 000310673600036 | - |
dc.identifier.bibliographicCitation | JOURNAL OF CLINICAL INVESTIGATION, v.122, no.11, pp.4077 - 4093 | - |
dc.relation.isPartOf | JOURNAL OF CLINICAL INVESTIGATION | - |
dc.citation.title | JOURNAL OF CLINICAL INVESTIGATION | - |
dc.citation.volume | 122 | - |
dc.citation.number | 11 | - |
dc.citation.startPage | 4077 | - |
dc.citation.endPage | 4093 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Research & Experimental Medicine | - |
dc.relation.journalWebOfScienceCategory | Medicine, Research & Experimental | - |
dc.subject.keywordPlus | TUMOR-INFILTRATING LYMPHOCYTES | - |
dc.subject.keywordPlus | ANTITUMOR IMMUNITY | - |
dc.subject.keywordPlus | VACCINE POTENCY | - |
dc.subject.keywordPlus | SELF-RENEWAL | - |
dc.subject.keywordPlus | HIGH NUMBER | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | AKT | - |
dc.subject.keywordPlus | ENHANCEMENT | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | RESISTANCE | - |
dc.subject.keywordAuthor | TUMOR-INFILTRATING LYMPHOCYTES | - |
dc.subject.keywordAuthor | CELL-LIKE PROPERTIES | - |
dc.subject.keywordAuthor | CERVICAL-CANCER | - |
dc.subject.keywordAuthor | ANTITUMOR IMMUNITY | - |
dc.subject.keywordAuthor | VACCINE POTENCY | - |
dc.subject.keywordAuthor | SELF-RENEWAL | - |
dc.subject.keywordAuthor | HIGH NUMBER | - |
dc.subject.keywordAuthor | RESISTANCE | - |
dc.subject.keywordAuthor | PATHWAY | - |
dc.subject.keywordAuthor | AKT | - |
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